The immune response is a complex and dynamic process initiated by infection, autoantigens, tumor-associated antigens and transplantation that involves antigen presenting cells (macrophages or dendritic cells), antigen-specific thymus-derived lymphocytes (T-cells) that can be further discriminated into helper or cytotoxic T-cells, and antibody forming cells of the B cell lineage. The helper T cells can be further differentiated into subsets termed Th1 that produce mostly interferon-γ (IFN-γ), or interleukin-2 (IL-2), and Th2 cells that produce mainly interleukin-4 (IL-4) or interleukin-5 (IL-5). The Th1 cells function predominantly in inflammatory reactions, where they recruit macrophages and other non-lymphoid cell types in the destruction of infectious agents. The Th2-type cells help principally in the production of antibodies through interactions with B cells, and this role predisposes to the development of asthma and allergic reactivity because of the generation of the reagenic antibody IgE (Wills-Karp, 1999, Ann. Rev. Immunol. 17:255–81).
The complex interactions among the distinct cell types are regulated by the secreted cytokines, and it is now recognized that functional balance between the two subsets of T-cells is important for normal immunity (Romagnani, 1997, Immunology Today 18: 263–266; Infante-Duarte et al., 1999, Immunopathol. 21:317–338). The definition of Th1 and Th2 helper T cells is an operational one based on expression of cytokines considered characteristic of the individual subsets, although non-lymphoid cells can produce certain essential cytokines. Often, both Th1 and Th2 responses are ongoing in particular infections, especially at later stages. Th1-type responses are generally protective against intracellular parasites; whereas extra cellular parasites are better counteracted by so-called Th0 T-cells producing both Th1 and Th2 cytokines, thus generating both cellular and humoral immunity. Optimal protection against metazoan parasites such as helminths is apparently conferred by Th2 responses. Th2-type responses favor HIV progression by allowing enhanced HIV replication in CD4+ T-cells, and a strong imbalance between Th1 and Th2-type cytokine production is observed in mice infected with defective leukemia virus, the so-called MAIDS model (Watson et al., 1995, J. Immunol. 155:2282–2291; U.S. Pat. No. 5,911,990 to Marchalonis et al.).
Polarized or unbalanced allergen-specific Th2 responses are responsible for initial triggering of allergic inflammation in atopic subjects. In general, polarization of Th1/Th2 cytokine expression induced by interaction of the pathogen with the host can lead to situations destructive to the host; i.e., the Th1–Th2 shift in MAIDS. However, correction of the imbalance can restore beneficial protection to the infected animal. Th1-dependent protection and Th2-mediated susceptibility is found in the response to the intracellular parasite Leishmania, and in leprosy, caused by Mycobacterium leprae. 
Thus, it would be beneficial to have compositions and methods for maintaining proper immune system functioning, i.e., proper amounts and ratios of cytokine production, in the presence of an underlying pathogenic condition. One molecule that provides for the proper functioning of the immune system and suppression of progression to AIDS in an immunodeficiency-type retrovirus-infected individual is described in U.S. Pat. No. 5,911,990 to Marchalonis et al. The molecule is a peptide that is derived from the T cell-receptor and has the amino acid sequence Cys Lys Pro Ile Ser Gly His Asn Ser Leu Phe Trp Tyr Arg Gln Thr (SEQ ID NO:1). This peptide was shown to suppress progression to AIDS and normalize aberrant Th1 and Th2 cytokine production in individuals infected with an immunodeficiency-type retrovirus.
Citation of a reference in this or in any section of the specification shall not be construed as an admission that such reference is prior art to the present invention.